端粒长度与2型糖尿病：孟德尔随机化研究与多基因风险评分分析

doi:10.16288/j.yczz.20-077

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Hereditas(Beijing) ›› 2020, Vol. 42 ›› Issue (9): 882-888.doi: 10.16288/j.yczz.20-077

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Telomere length and type 2 diabetes: Mendelian randomization study and polygenic risk score analysis

Lan Cao^1,³, Zhiqiang Li^2,³, Yongyong Shi³, Yun Liu⁴

^1. Shanghai Center for Women and Children’s Health, Shanghai 200062, China;
^2. The Affiliated Hospital of Qingdao University, The Biomedical Sciences Institute of Qingdao University (Qingdao Branch of SJTU Bio-X Institutes), Qingdao University, Qingdao 266003, China
^3. Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200030, China
^4. Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China;

Received:2020-03-18 Revised:2020-05-22 Online:2020-09-20 Published:2020-08-28
Supported by:
Supported by Foundation of Shanghai Municipal Health Commission No(20164Y0163)

Abstract

Abstract:

Recent epidemiological studies suggest an association between shorter telomere length and higher risk for type 2 diabetes (T2D). However, results from observational studies are susceptible to confounding and reverse causation, and it is not clear whether there is a causal association between telomere length and T2D. Using Mendelian randomization (MR) and polygenic risk score (PRS) approaches, we had evaluated the causal effect of telomere length on T2D in the Chinese Han population. Using 8 telomere-length associated genetic variants as instrumental variables, an analysis of genetically predicted telomere length and T2D risk was performed in the MR study based on data from a T2D genome-wide association study (GWAS) in 2632 individuals (1318 cases and 1314 controls). We also applied a PRS approach to investigate the causal relationship using Chinese GWAS data. The inverse-variance weighted, MR-Egger regression, simple median, and weighted median methods yielded no evidence of association between genetically predicted longer telomere length and risk of T2D (OR = 0.78, 95% CI: 0.36 ~ 1.68, P = 0.522; OR = 0.23, 95% CI: 0.01 ~ 7.64, P = 0.412; OR = 0.60, 95% CI: 0.28 ~ 1.28, P = 0.185; OR = 0.64, 95% CI: 0.31 ~ 1.33,P = 0.233; respectively). Further, PRS analysis did not produce consistent genetic overlap between telomere length and T2D. Accordingly, this study found no evidence supporting a causal association between telomere length and T2D. Further studies with larger cohorts could yield more reliable results and conclusions.

Key words: Mendelian randomization, polygenic risk score, telomere length, type 2 diabetes

Lan Cao, Zhiqiang Li, Yongyong Shi, Yun Liu. Telomere length and type 2 diabetes: Mendelian randomization study and polygenic risk score analysis[J]. Hereditas(Beijing), 2020, 42(9): 882-888.

Figures/Tables 3

References 32

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SNP	Chr.	临近基因	效应等位基因	MAF	端粒长度		T2D
SNP	Chr.	临近基因	效应等位基因	MAF	β^*	P值	β	P值
rs10936599	3	TERC	C	0.252	0.117	2.54×10^-31	-0.038	0.53
rs2736100	5	TERT	C	0.486	0.094	4.38×10^-19	-0.053	0.37
rs7675998	4	NAF1	G	0.217	0.090	4.35×10^-16	-0.077	0.32
rs4387287	10	OBFC1	A	NA	0.100	2.33×10^-11	-0.114	0.17
rs8105767	19	ZNF208	G	0.291	0.058	1.11×10^-09	-0.027	0.69
rs755017	20	RTEL1	G	0.131	0.074	6.71×10^-09	0.095	0.12
rs3027234	17	CTC1	C	0.179	0.057	2.29×10^-08	-0.323	0.04
rs11125529	2	ACYP2	A	0.142	0.067	4.48×10^-08	0.135	0.08

Telomere length and type 2 diabetes: Mendelian randomization study and polygenic risk score analysis

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